The Physiologic Steps to Muscle Contraction
This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP.
Troponin is a complex of three proteins that are integral to muscle contraction. Troponin is attached to the protein tropomyosin within the actin filaments, as seen in the image below. When the muscle is relaxed tropomyosin blocks the attachment sites for the myosin cross bridges (heads), thus preventing contraction. When the muscle is stimulated to contract by the nerve impulse, calcium channels open in the sarcoplasmic reticulum (which is effectively a storage house for calcium within the muscle) and release calcium into the sarcoplasm (fluid within the muscle cell). Some of this calcium attaches to troponin which causes a change in the muscle cell that moves tropomyosin out of the way so the cross bridges can attach and produce muscle contraction. In the gym or during exercise virtually all muscular fatigue occurring is energy system fatigue. That is, the rate of work within the muscle can not be maintained because ATP (energy) can no longer be provided. Strength and hypertrophy (training to make muscles stronger or bigger) training are prime examples of the types of training that can cause muscle failure due to energy system fatigue.
Still, its constituents are rather easy to remember, as there are only two of them. The connection between size and types is also clear. If the constitutes are large, the motor unit is also large and fast. The contradiction can provide an example: the eyes and extraocular muscles are small, so the units are fast. If motor neurons and muscle fibers are small, the motor unit is small and slow. The back and postural muscles in it are big, so the units are slow. Dealing with slow and fast motor units, it is critical to remember two opposites, slow-oxidative and fast-glycolytic. The intermediate part will have the characteristics of both of them and can be easily recollected when combining the names of these two: fast (glycolytic) + (slow) oxidative = fast-oxidative.
ACh is the neurotransmitter that binds at the neuromuscular junction (NMJ) to trigger depolarization, and an action potential travels along the sarcolemma to trigger calcium release from SR. The actin sites are exposed after Ca++ enters the sarcoplasm from its SR storage to activate the troponin-tropomyosin complex so that the tropomyosin shifts away from the sites. The cross-bridging of myosin heads docking into actin-binding sites is followed by the “power stroke”—the sliding of the thin filaments by thick filaments. The power strokes are powered by ATP. Ultimately, the sarcomeres, myofibrils, and muscle fibers shorten to produce movement.
Floeter, Mary. Structure and Function of Muscle Fibers and Motor Units 2010. Web.
McDonnall, Daniel, Gregory Clark, and Richard Normann. “Selective Motor Unit Recruitment via Intrafascicular Multielectrode Stimulation.” Canadian Journal of Physiology and Pharmacology 82.8-9 (2004): 599-609. Print.
Motor Units. n.d. Web.